Sucralfate

Denis M. McCarthy, M.D., M.Sc.

N Engl J Med 1991; 325:1017-1025October 3, 1991DOI: 10.1056/NEJM199110033251407
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Letters
John A. Oates, M.D., Editor Alastair JJ. Wood, M.D., Associate Editor j
THE past 10 years have witnessed major changes in our understanding of the
pathogenesis and treatment of what are commonly called the acid-peptic diseases.
Schwarz's dictum "without acid gastric juice, no peptic ulcer" still applies.1
Increasingly, however, ulcers have come to be seen as areas of mucosa in which the
effects of all noxious influences have exceeded the restorative capacities of all processes
favorable to mucosal repair and integrity. A major stimulus to the growth of our
knowledge in this area has been the development of drugs that have little or no effect on
intragastric acidity, yet that have a clear ability to heal ulcers through mucosal protective
effects. Chief among these is sucralfate.

Chemistry
Sucralfate (Carafate, Marion Merrell Dow, Kansas City, Mo.) is a complex salt of sucrose
sulfate and aluminum hydroxide; its structure is shown in Figure 1Figure 1

The Structure of Sucralfate.. It is very poorly soluble in water, a

property that greatly limits experiments aimed at determining its mode of action. It is
minimally soluble in dilute acid (e.g., gastric juice) and in alkali, and when dissolved it
breaks down into its aluminum salt and sucrose sulfate, which form a polyanion gel-like
substance.2 Whether its biologic properties derive from the undissolved or the dissolved
form is uncertain. Taken by mouth, the tablet disintegrates in the stomach and in the
presence of acid forms a viscous suspension that binds with high affinity to both
defective and normal mucosa. The compound was developed during studies of sulfated
polysaccharides (such as amylopectin or pepstatin) that bind pepsins but lack antiulcer
efficacy.3 However, many such complex synthetic carbohydrates proved to have systemic

anticoagulant (heparin-like) and colitis-inducing (carrageenan-like) effects and were

withdrawn from use. The simplification of the carbohydrate molecule to sucrose, its
sulfation, and its conjugation with a basic aluminum salt resulted in a pepsin-inhibiting
molecule free of these effects.
In the presence of acid, the compound releases aluminum, acquires a strong negative
charge, and binds electrostatically to any positively charged chemical groups in its
environment, including proteins, peptides, drugs, metals, and large molecules such as
mucins (glycoproteins and glycolipoproteins); with mucins it may form complex gels
with various types of cross-linkage. Its physical, mechanical, adsorbent, ion-exchange,
and buffering properties may all contribute to mucosal protection.

Clinical Pharmacology
Because of its poor solubility, little sucralfate is absorbed from the gastrointestinal tract
(mostly as the intact sulfated disaccharide, which is then excreted in the urine). No
systemic toxicity, tumorigenicity, teratogenicity, or any effects on pregnancy or
reproduction due to the intact molecule have been found in humans or animals. Studies in
animals using oral doses of up to 1 g per kilogram of body weight failed to establish a
lethal dose.4
Aluminum absorption during sucralfate therapy is comparable to that during treatment
with aluminum hydroxide.5 6 7 The theoretical aluminum content of sucralfate
(molecular weight, 2385) ranges from 18.2 to 20.7 percent by weight in different batches,
and a dose of 1 g four times daily provides 728 to 828 mg of aluminum for absorption
(data obtained from Marion Merrell Dow Laboratories). Although over 98 percent of this
is eliminated in feces, urinary aluminum excretion rises 10-fold during sucralfate
administration in subjects with normal renal function.7
Although plasma levels of aluminum in normal subjects are generally believed not to rise
during up to 12 months of sucralfate therapy,8 9 10 in two recent studies substantial
increases were found in normal subjects after 2 to 21 days of sucralfate (4 g per day).11 ,
12 Plasma aluminum levels do increase in a dose-dependent manner in sucralfate-treated
patients undergoing dialysis,7 , 13 and aluminum intoxication has developed in at least
four such patients during sucralfate therapy 7 , 14 15 16 Statements that sucralfate may be
"the phosphate-binding agent of choice" in patients with uremia who have ulcers should
be taken with some caution5 , 7 , 13 , 17; like aluminum-containing antacids, sucralfate
can cause severe hypophosphatemia.18 The problem of aluminum retention is likely to be
negligible except perhaps in long-term users with renal insufficiency, especially those
undergoing dialysis.5 , 7 , 14 15 16 Controversy continues over whether the increased
brain levels of aluminum in patients with Alzheimer's disease are linked to the
consumption of antacid or that of sucralfate.19

Actions

Several different actions combine to enable sucralfate to prevent acute mucosal injury,
reduce inflammation, and heal existing ulcers. A detailed discussion of these actions is
beyond the scope of this article, but the topic has been reviewed extensively.2 , 3 , 20 , 21
The actions that reduce the effect of factors injurious to the mucosa or that favor healing

are shown in Table 1Table 1

Possible Actions of Sucralfate.. Overall, the
major drug actions of sucralfate that contribute to clinical efficacy are likely to include
the inhibition of peptic digestion (especially by pepsin A); the many effects on the output,
chemical composition, physical structure, and resistance to degradation of the mucus gel
layer; the stimulation of prostaglandin release and all the biologic processes thus
activated (bicarbonate secretion, mucus production, blood flow, cell division, and the
like); the stimulation of prostaglandin-independent output of mucus and bicarbonate; and
the resultant effects on the protection of the mucosal proliferative zone, the facilitation of
mucosal restitution and cell division, and the stimulation of repair and healing by a
variety of mechanisms. Many of these processes may be interrelated: the effects on
arachidonic acid shown in Table 1, for instance, may trigger the effects on mucus,
bicarbonate output, and tissue growth, regeneration, and repair. The principal mode or
modes of action may vary in different organs and species, and some of the actions listed
in the table may be the consequences of a basic action that is as yet unrecognized. No
single principal action can be identified at this time.

Safety and Side Effects

In 10 years of use, sucralfate has proved remarkably safe,46 , 47 although no major
studies of safety have been performed since marketing began. In placebo-controlled
studies, the most common side effect was constipation, which occurred in 0 to 15 percent
of patients (usual range, 1 to 3 percent). Other side effects, occurring in 0 to 5 percent,
included dry mouth, nausea, vomiting, headache, urticaria, and rashes. Sucralfate has
rarely been discontinued because of side effects. Exceptionally rare side effects are
gastric bezoar formation,48 51 aluminum intoxication,7 , 14 16 and hypophosphatemia.18
There have been no prospective safety studies in pregnant or lactating women, children,
or the elderly.

Drug Interactions
When the following drugs are administered with sucralfate, the absorption and
bioavailability of single doses are substantially reduced: ciprofloxacin,52 55
norfloxacin,56 , 57 theophylline,58 , 59 tetracycline,60 aminophylline,60 phenytoin,60 62
digoxin,60 , 63 and amitriptyline.64 The bioavailability of digoxin, tetracycline, and
phenytoin was not reduced when they were given two hours before sucralfate.60 , 63 At
present sucralfate should not be used if fluoroquinolone antibiotics are required.53 The

effects of long-term administration of these drugs during sucralfate therapy have not been
studied.
The ability of sucralfate to delay slightly the absorption of cimetidine and ranitidine,
though of some pharmacokinetic interest,65 71 is not clinically important; interactions
with other H2-antagonists or omeprazole have not been studied. Some drugs whose
bioavailability is not influenced substantially by administration in combination with
sucralfate include acetaminophen, aspirin, diazepam, erythromycin, ethinyl estradiol,
ibuprofen, imipramine, indomethacin, ketoprofen, naproxen, prednisone, propranolol,
quinidine, and warfarin. The effect of combined therapy with antacids has not been
evaluated in humans; in animals, antacids given shortly (15 minutes) before sucralfate
diminish its binding to gastric ulcers.72

Efficacy in Clinical Trials

Sucralfate has been approved by the Food and Drug Administration to treat acute
duodenal ulcers, and as long-term maintenance therapy to prevent their recurrence.
Confident of its safety, practitioners have used the drug for many other conditions. In
most areas of interest, many of the clinical trials have been less than definitive, in the
sense that they are open, single-blind, of uncertain randomization, or lacking in outcome
criteria, and very often published in commercially sponsored journal supplements.

Duodenal Ulcer
In the five randomized, double-blind, and interpretable trials conducted to date,73 77 a
total of 213 patients treated with sucralfate (1 g four times a day the FDA-approved
dose) were compared with 217 placebo-treated patients. The average rates of healing,
weighted for sample size, in the patients treated with sucralfate were 34.7 percent (after 2
weeks in two trials), 77 percent (after 4 weeks in three trials), 60 percent (after 6 weeks in
one trial), 82 percent (after 8 weeks in one trial), and 77 percent (after 12 weeks in one

trial)74 77 (Table 2Table 2

Randomized, Double-Blind Trials of
Sucralfate in Patients with Duodenal Ulcers.). In all, sucralfate was significantly better
than placebo. The rates of healing in the placebo-treated patients also varied considerably,
with the highest rates in the two U.S. studies74 , 75 (58 and 64 percent healing after four
weeks) and the lowest in China (25 percent after four weeks)77 and South Africa (24
percent after six weeks). This variation probably derives from the fact that unrestricted
antacid use was allowed in both U.S. studies. Although low-dose antacid therapy is no
longer regarded as ineffective in ulcer healing, antacid use should have been of equal
benefit in both arms of each trial. Hence, although the superiority of sucralfate over
placebo is unequivocal, the rate of healing due to sucralfate alone has not been
established.

There have been six randomized, double-blind, controlled trials comparing sucralfate and
cimetidine78 83 (Table 2). In these, the rate of healing in a total of 324 patients treated
with sucralfate (1 g four times a day) was compared with that in 334 patients treated with
cimetidine (800 to 1200 mg per day). The average healing rates in 278 patients treated
with sucralfate were 73 percent (after 4 weeks in six trials) and 87 percent (after 8 weeks
in four trials), as compared with 77 percent and 91 percent, respectively, in 262
cimetidine-treated patients. In 10 additional open or single-blind studies of sucralfate ( 1
g four times a day), 1 in comparison with ranitidine84 and 9 in comparison with
cimetidine,85 93 the healing rates were similar.

Smoking and Ulcer Healing

Lam et al. have claimed that duodenal-ulcer healing was delayed in smokers treated with
H2-antagonist agents but not sucralfate.85 This study was not stratified according to
smoking status or ulcer size (ulcers are known to be larger in smokers), was not
doubleblind or placebo-controlled, and did not prohibit or record the consumption of
alcohol, analgesics, or traditional Chinese ulcer remedies, and thus it has been subjected
to serious criticism.94 Some studies lend support to Lam's claim,95 but others do not.78 ,
96 98 In a recent randomized, double-blind trial comparing sucralfate and placebo in 293
patients in Canada, patients who smoked had significantly lower healing rates after four
and eight weeks than those who did not, regardless of treatment group.97 Furthermore, a
meta-analysis of the outcome of therapy in 4451 patients from 30 trials (involving 64
treatment groups and 15 placebo groups) that met predetermined criteria for inclusion did
not show any advantage for sucralfate or reveal impaired healing in patients taking any
other drug, once the rates were corrected for the effect of smoking on healing in the
placebo-treated patients99

Relapse Rates after Healing in Patients Treated with Sucralfate

A final issue is whether patients with duodenal ulcers that healed with sucralfate have
lower relapse rates than patients treated with H2-antagonist drugs.95 Although
retrospective analysis and inappropriate pooling of data from a number of studies not
designed to assess the issue95 support a possible advantage for sucralfate, no valid
conclusion can be drawn from this analysis. The question needs to be addressed in a large
prospective study that is carefully stratified to ensure that other risk factors (i.e., ulcer
size, number of cigarettes smoked per day, infection with Helicobacter pylori, exposure
to analgesic agents, acid output, and presence of antral gastritis) are evenly distributed.

Maintenance Therapy for Duodenal Ulcers

The efficacy of sucralfate (2 g per day) in preventing the recurrence of duodenal ulcers
has recently been reviewed.100 In five randomized, placebo-controlled, double-blind 12month trials,10 , 101 104 the weighted average 12-month recurrence rates as assessed by
endoscopy were 38 percent in 150 patients treated with sucralfate and 70 percent in
patients given placebo. In one of those studies,101 in which the 12-month recurrence rate
was 27 percent in patients treated with sucralfate as compared with 81 percent in patients

given placebo, "erosions or superficial ulcers" were not considered recurrences. In a

recent randomized, double-blind four-month study of 122 patients,105 endoscopy was
performed monthly and whenever symptoms recurred. By the fourth month, ulcers had
recurred in 55 percent of the placebo-treated and 36 percent of the sucralfate-treated
patients, as shown by cumulative point-prevalence analysis, and in 63 and 42 percent,
respectively, on the basis of life-table estimates.105 Sucralfate (1 g twice a day) is now
approved for maintenance therapy by the FDA.
One moderate-sized study in Japan106 compared the rate of ulcer recurrence in patients
taking sucralfate (2 g per day) with that in patients taking cimetidine (400 mg per day) or
a combination of both drugs. After one year the recurrence rates were similar: 60 percent
in patients taking cimetidine, 58 percent in patients taking sucralfate, and 52 percent in
patients taking both drugs. In four small single-blind studies104 , 107 109 of maintenance
therapy with sucralfate (2 g per day) or H2-antagonist agents, cimetidine (400 mg at
bedtime; 79 patients) and ranitidine (150 mg at bedtime; 15 patients), no clinically
important or statistically significant differences emerged. Thus, sucralfate and
H2antagonists are better than placebo, but on the basis of the small numbers treated with
sucralfate, it cannot yet be concluded that they are equally effective.

Gastric Ulcer
Two placebo-controlled trials have assessed the efficacy of treatment with sucralfate (4 g
per day) for eight or more weeks in patients with gastric ulcers.110 , 111 The rates of
healing were 60 percent for sucralfate and 42 percent for placebo (P<0.05) after eight
weeks in one study.110 In the second study, the benefit varied with the type of ulcer;
sucralfate was no better than placebo in patients with gastric ulcers associated with
duodenal ulcers.111 However, ulcers of the gastric corpus healed in 80 and 90 percent of
the sucralfate-treated patients after 8 and 12 weeks, respectively, as compared with 40
and 52 percent of the patients given placebo after the corresponding intervals (P<0.001);
prepyloric ulcers also healed well with sucralfate.111
The healing of gastric ulcers in patients treated with sucralfate (4 g per day) or cimetidine
(800 mg per day) has been compared in four trials.81 , 112 114 The average healing rates
(weighted for sample size) at 4, 8, and 12 weeks, respectively, were 57, 88, and 96
percent for sucralfate and 65, 88, and 94 percent for cimetidine. Four additional singleblind or nonrandomized studies showed similar healing rates.86 , 91 , 96 , 115 Two studies
comparing sucralfate and ranitidine116 , 117 showed no differences between the two
treatments. In one study sucralfate was superior to low-dose antacids after four and eight
weeks of therapy.118 Sucralfate has not been approved by the FDA for either acute or
maintenance therapy of gastric ulcers.

Prevention of Recurrences of Gastric Ulcers

Of seven studies of the efficacy of sucralfate in preventing a recurrence of gastric ulcers,
four indicated a benefit of the drug.106 , 116 , 119 123 In a small but well-executed
randomized, double-blind, placebo-controlled 6-month study in South Africa,122 the

relapse rate was 16 percent in the patients treated with sucralfate (1 g in the morning plus
2 g at night), as compared with 70 percent in those given placebo (P<0.001); most
relapses were symptomatic, since the only endoscopy was performed at 24 weeks. In 127
patients treated for 12 months with sucralfate (2 g per day), cimetidine (400 mg at
bedtime), or both who underwent endoscopy every 3 months, the endoscopically
determined relapse rates after 12 months were 20 percent for sucralfate, 27 percent for
both drugs, and 55 percent for cimetidine106; the rates for the first two treatments were
significantly different (P<0.01) from the rate for cimetidine alone, but not from each
other. A comparison of sucralfate (1 g twice a day) and ranitidine (150 mg at bedtime) in
groups of 18 subjects each, with endoscopy carried out every 6 months and whenever
symptoms recurred,116 revealed relapse rates after 12 months of 44 percent for sucralfate
and 50 percent for ranitidine. Finally, in a large 12-month study, sucralfate (1 g three
times a day in 175 subjects) was compared with ranitidine (150 mg at bedtime in 171
subjects). The recurrence rates for ranitidine after 9 and 12 months (18 percent and 21
percent, respectively) were significantly lower than for sucralfate (30 percent and 30
percent, P<0.05).123 Because no placebo groups were included in the studies comparing
sucralfate and H2-antagonists, the efficacy of sucralfate in preventing recurrences of
gastric ulcers is not known, and its use cannot be recommended at this time.

Gastrointestinal Bleeding
Peptic Ulcer
In most patients with bleeding peptic ulcers, the bleeding stops spontaneously and the
patients do not have further episodes of bleeding; no form of pharmacologic therapy has
altered these short-term outcomes.124 In long-term maintenance studies, only ranitidine
has been reported to reduce the recurrence of bleeding over a three-year period of followup.125 At present, the benefit of sucralfate in patients with bleeding ulcers lies in treating
the ulcers and not the bleeding.

Stress-Related Mucosal Disease

Whether or not various treatments prevent bleeding from stress ulcers (also termed stressrelated mucosal disease, hemorrhagic gastritis, and stress bleeding) has been the subject
of controversy.126 , 127 A meta-analysis of 42 randomized trials, selected according to
prospectively defined criteria and involving 4409 patients at risk, demonstrated that in
reducing the risk of overt bleeding, antacids and H2-antagonist drugs were superior to
placebo or no therapy. Likewise, H2-antagonists were superior to antacids, and
pirenzepine (an M2-muscarinicreceptor antagonist) was superior to H2-antagonists.128
H2-antagonists were also more effective than antacids in reducing clinically important
bleeding (involving hemodynamic instability, a fall in the hemoglobin level by more than
30 g per liter, and a requirement for transfusion).128
The claims for the efficacy of sucralfate are based not on placebo-controlled studies, but
on studies in which sucralfate appeared as effective as antacids and H2-antagonists.127 It
appears unwise to assess efficacy until larger prospective, placebo-controlled trials are

conducted. Different forms of sucralfate were used in different doses (e.g., 4, 6, or 9 g per
day), different volumes (from 5 to 20 ml), and different formulations in the various trials.
The mortality rate in patients with stress-induced bleeding that is treated with H2antagonists (seven trials) or antacids (two trials) has not been lower than in untreated
patients.126 Of eight trials comparing mortality rates in sucralfate-treated patients with
those in patients treated with H2-antagonists or antacids, seven showed no statistically
significant benefit for sucralfate.126 One was said to show lower mortality,126 but the
original study claimed that the trend was not statistically significant (P = 0.07).129 In
mortality studies of critically ill patients with a variety of severe illnesses, mathematical
associations derived from retrospective analyses do not establish that differences in
mortality are attributable to drug therapy.

Combined Therapy with H2-Antagonist Drugs

Of particular interest is therapy combining sucralfate and an H2-antagonist drug. No
controlled studies show a statistically significant benefit of therapy involving a
combination of sucralfate and any H2-antagonist, as compared with either drug alone, in
treating acute duodenal ulcer, in ulcer maintenance therapy, in stress bleeding, or in reflux
esophagitis. Despite the lack of evidence of superior efficacy of combination therapy, its
use continues.

Nosocomial Pneumonia
A major controversy surrounding the prophylactic use of sucralfate for patients in the
intensive care unit has arisen from claims that sucralfate was associated with a lower risk
of nosocomial pneumonia than pH-elevating antacids or H2-antagonist drugs.126 , 129 ,
130 Pulmonary infections are common in patients with indwelling stomach tubes who are
receiving antacids, particularly during mechanical ventilation.131 , 132 A retrospective
study of risk factors for pneumonia in 233 patients receiving mechanical ventilation
showed an odds ratio of 2.5 (95 percent confidence interval, 1.2 to 5.0) for cimetidine use
as a risk factor; whether this association was causal or whether it simply reflected the use
of cimetidine in the sickest patients was not evaluated.133
Two prospective studies have compared the risk of nosocomial pneumonia in patients
receiving mechanical ventilation who were treated with sucralfate with the risks in
similar patients treated with antacids134 or with either antacids or H2-antagonists.129 In
the first study, pneumonia developed in more patients treated with antacids than patients
treated with sucralfate (34 vs. 10 percent, P<0.05).134 The results of the second study
were similar, but the difference was not significant (23 vs. 12 percent for the risks with
antacids and sucralfate, respectively); the lowest risk (6 percent) was found with the use
of H2-antagonists.129 By grouping antacids and H2-antagonists together as alkalinizing
agents and excluding from the analysis six patients who were changed to the opposite
treatment, the authors claimed that sucralfate was less hazardous than therapy with
antacids or H2-antagonists when these treatment groups were combined (P = 0.05).

Despite considerable informed criticism,135 , 136 this invalid conclusion with regard to
H2-antagonists has been widely publicized in marketing sucralfate.
Whether nosocomial pneumonia more often accompanies the use of H2-antagonists or
that of sucralfate is clinically important. In one well-designed trial, a continuous infusion
of cimetidine (900 mg per day in 56 patients) was compared with an infusion of placebo
(in 61 patients)137; placebo, but not cimetidine, was associated with nosocomial
pneumonia. In another trial, an infusion of cimetidine (900 mg per day) was compared
with a sucralfate suspension ( 1 g four times daily); the rates of bleeding, pneumonia, and
mortality did not differ significantly between groups.138 Finally, a meta-analysis of
outcomes in 493 patients revealed that prophylaxis for stress ulcers with drugs that raised
the intragastric pH did not increase the incidence of pneumonia in comparison with
placebo or no therapy.139
That sucralfate is safer than antacids appears likely; the reason is less clear. Previous
studies advanced the hypothesis that as gastric pH values increase above 3.5, gramnegative flora increase in the stomach, and their aspiration would then lead to
pneumonia.134 High pH values should thus be found mainly in patients treated with
antacids or H2-antagonists, but not in those treated with sucralfate. No actual values for
intragastric pH were reported, but from one study134 it can be calculated that the pH
exceeded 3.5 in 77 percent of the sucralfate-treated patients and 4.5 in 54 percent, casting
doubt on the hypothesis that differences between sucralfate and other agents, if they exist,
can be explained by sucralfate's lack of effect on gastric pH.127 In fact, patients in the
intensive care unit, especially those with hypotension, frequently have diminished output
of gastric acid,140 , 141 and increased acid secretion can be demonstrated consistently
only in patients with intracranial lesions.142 More recently, sucralfate has been reported
to have activity against both gram-negative and gram-positive organisms in the gastric
contents of patients in the intensive care unit126 , 143 , 144 an effect beyond that
assumed in the biologic hypothesis linking nosocomial pneumonia with reduced gastric
acidity.
In summary, nosocomial pneumonia appears to be associated less frequently with
sucralfate than with antacid therapy; whether this is due to an increased risk with antacids
or a reduced risk with sucralfate is unknown. The risk of nosocomial pneumonia is not
increased by H2-antagonists as compared with placebo, and to date no studies have
established that the risk is lower with sucralfate than with H2-antagonists.

Miscellaneous Uses
In patients with duodenal but not gastric ulcers associated with the use of nonsteroidal
antiinflammatory drugs (NSAIDs), the ulcers are equally likely to be healed with
sucralfate (1 g four times daily) or ranitidine (150 mg twice daily), whether or not the
NSAID therapy is continued.93 , 145 147 Sucralfate is significantly superior to placebo in
reducing the frequency148 and intensity148 , 149 of dyspeptic symptoms during NSAID
therapy. It does not appear to prevent NSAID-associated gastric or duodenal ulcers or
their complications, nor does it lower the associated morbidity and mortality.147

Sucralfate has no demonstrated place in the prevention or therapy of an NSAIDassociated gastric ulcer or its complications.147 , 150 152
More than 20 clinical trials have evaluated sucralfate therapy in patients with
gastroesophageal reflux disease. Among the controlled studies, only one comparison of
sucralfate with placebo showed a significant reduction of symptoms,153 and one showed
significantly better healing with sucralfate than with placebo.154 Overall, when
comparisons of active treatment with H2-antagonists or open-label studies are included,
the drug seems modestly effective in nonerosive esophageal disease. Controlled trials of
its efficacy in healing after sclerotherapy and the treatment of other esophageal ulcers
show no benefit.155 , 156
Nearly 15 publications, mostly anecdotal or uncontrolled, attest to the value of topical
sucralfate in preventing or treating stomatitis or proctitis induced by chemotherapy or
radiation. Two show significant benefit in stomatitis.157 , 158 Despite anecdotal claims
of efficacy, two controlled trials have failed to show a benefit from sucralfate enemas in
inflammatory bowel disease, and sucralfate proved inferior to enemas using 5aminosalicylic acid or prednisone. Anecdotal reports of benefit in the healing of
decubitus ulcers or inflamed perianal skin and in prophylactic use to prevent gastric
bleeding from high-dose steroids deserve further evaluation. Future applications of
sucralfate have been reviewed by Tytgat.159

Conclusions
Sucralfate appears to be safe and effective in the treatment of patients with duodenal or
gastric ulcers. Reports of lower relapse rates for ulcers after the discontinuation of
sucralfate therapy than after H2-antagonist drug therapy cannot be accepted until this
issue has been examined in controlled trials. Maintenance therapy with sucralfate is
effective in duodenal ulcers, but it may not be as effective as therapy with H2-antagonist
drugs. Sucralfate appears effective in preventing stress bleeding in patients receiving
mechanical ventilation, but it has no demonstrated advantage over H2-antagonist drugs.
Other uses are largely unconfirmed or experimental and should be evaluated by formal
studies.